Antitumor actions of cytokines on new human papillary thyroid carcinoma cell lines.

Ohta, Kazuyasu; Pang, Xuan-Ping; Berg, Loretta; Hershman, Jerome M.

doi:10.1210/jcem.81.7.8675585

Cited by 29 publications

(23 citation statements)

References 14 publications

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“…However, only a few normal thyroid cell lines (Weiss et al 1984b, Berlingieri et al 1993, Venkataraman et al 1998) and thyroid cancer cell lines (Ohta et al 1996, Kogai et al 2001 express endogenous NIS in response to TSH stimulation. Most of these thyroid cell lines have de-differentiated and lost expression of TSH-R and TTF-1, which are expressed in most differentiated thyroid cancers.…”

Section: Thyroid Cancer Modelsmentioning

confidence: 99%

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

Kogai¹,

Taki²,

Brent³

2006

Endocr Relat Cancer

168

150

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The sodium/iodide symporter (NIS) mediates iodide uptake in the thyroid gland and lactating breast. NIS mRNA and protein expression are detected in most thyroid cancer specimens, although functional iodide uptake is usually reduced resulting in the characteristic finding of a 'cold' or non-functioning lesion on a radioiodine image. Iodide uptake after thyroid stimulating hormone (TSH) stimulation, however, is sufficient in most differentiated thyroid cancer to utilize b-emitting radioactive iodide for the treatment of residual and metastatic disease. Elevated serum TSH, achieved by thyroid hormone withdrawal in athyreotic patients or after recombinant human thyrotropin administration, directly stimulates NIS gene expression and/or NIS trafficking to the plasma membrane, increasing radioiodide uptake. Approximately 10-20% differentiated thyroid cancers, however, do not express the NIS gene despite TSH stimulation. These tumors are generally associated with a poor prognosis. Reduced NIS gene expression in thyroid cancer is likely due in part, to impaired trans-activation at the proximal promoter and/or the upstream enhancer. Basal NIS gene expression is detected in about 80% breast cancer specimens, but the fraction with functional iodide transport is relatively low. Lactogenic hormones and various nuclear hormone receptor ligands increase iodide uptake in breast cancer cells in vitro, but TSH has no effect. A wide range of 'differentiation' agents have been utilized to stimulate NIS expression in thyroid and breast cancer using in vitro and in vivo models, and a few have been used in clinical studies. Retinoic acid has been used to stimulate NIS expression in both thyroid and breast cancer. There are similarities and differences in NIS gene regulation and expression in thyroid and breast cancer. The various agents used to enhance NIS expression in thyroid and breast cancer will be reviewed with a focus on the mechanism of action. Agents that promote tumor differentiation, or directly stimulate NIS gene expression, may result in iodine concentration in 'scan-negative' thyroid cancer and some breast cancer.

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Section: Thyroid Cancer Modelsmentioning

confidence: 99%

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

Kogai¹,

Taki²,

Brent³

2006

Endocr Relat Cancer

168

150

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“…The ARO and FRO cells derived from a human anaplastic thyroid carcinoma, BCPAP, TPC-1, and BHP 17-10 derived from poorly differentiated papillary thyroid carcinoma, and FTC-133 cells derived from a follicular thyroid cancer were grown as previously described (Hoelting et al 1995, Ohta et al 1996, Russo et al 2001. Control cells were exposed to DMSO alone at the same concentration present in cultures exposed to the test compounds (i.e., 1:5000 -0.02% when final concentrations of 10 mM/l compounds were used).…”

Section: Cell Cultures and Cell Growth Analysismentioning

confidence: 99%

Cytotoxic effects of a novel pyrazolopyrimidine derivative entrapped in liposomes in anaplastic thyroid cancer cells in vitro and in xenograft tumors in vivo

Celano¹,

Schenone²,

Cosco³

et al. 2008

Endocrine Related Cancer

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In this study, we evaluated the activity of two novel pyrazolopyrimidine derivatives (Si 34 and Si 35) against ARO cells, a human anaplastic thyroid cancer cell line. ARO cells exposed to different concentrations of the drugs showed a reduced growth rate and an increase of mortality. After 72 h incubation, doses of 5 and 10 mM Si 34 determined a decrease of cell counts by w25% and w75% compared with those of control cells respectively. Similar findings were observed using Si 35. Treatment with both Si 34 and Si 35 at 10 mM increased cell mortality also (w29% and w18% respectively). At these concentrations, a decrease in cyclin D1 levels was observed. To improve the biopharmaceutical properties, a liposome formulation was prepared. When entrapped in unilamellar liposomes, Si 34 exerted its cytotoxic effects even at lower doses (maximal inhibition at 5 mM) and after shorter incubation time (48 h) either in ARO or other thyroid cancer cell lines. The effects were associated with weak apoptotic death. Inhibition of epidermal growth factorstimulated src and ERK phosphorylation, as well as reduction of migration properties of ARO cells was also observed. Moreover, the growth of tumor xenografts induced in severe combined immunodeficiency (SCID) mice was inhibited by i.v. administration of 25-50 mg/kg of the drug liposomal formulation. In conclusion, the liposomal preparation of this novel pyrazolopyrimidine derivative appears to be a promising tool for the treatment of anaplasic thyroid cancer.

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“…The papillary thyroid carcinoma cell lines BHP-2, BHP-5, BHP-7, BHP-10, BHP-14, BHP-17, BHP-18, and BHP-19 were generous gifts from Dr. Jerome M. Hershman (West Los Angeles Veterans Affairs Medical Center, Los Angeles, CA; refs. 15,16). The SW579 cell line, derived from a poorly differentiated human thyroid adenocarcinoma (poorly differentiated carcinoma with nuclear features of papillary carcinoma and squamous differentiation), and the TT cell line, derived from a medullary thyroid carcinoma, were purchased from American Type Culture Collection (Manassas, VA).…”

Section: Human Tissuesmentioning

confidence: 99%

Targeting BRAFV600E in thyroid carcinoma: therapeutic implications

Mitsiades

Negri

McMullan

et al. 2007

Molecular Cancer Therapeutics

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B-Raf is an important mediator of cell proliferation and survival signals transduced via the Ras-Raf-MEK-ERK cascade. BRAF mutations have been detected in several tumors, including papillary thyroid carcinoma, but the precise role of B-Raf as a therapeutic target for thyroid carcinoma is still under investigation. We analyzed a panel of 93 specimens and 14 thyroid carcinoma cell lines for the presence of BRAF mutations and activation of the mitogen-activated protein/ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway. We also compared the effect of a B-Raf small inhibitory RNA construct and the B-Raf kinase inhibitor AAL881 on both B-Raf wild-type and mutant thyroid carcinoma cell lines. We found a high prevalence of the T1799A (V600E) mutation in papillary and anaplastic carcinoma specimens and cell lines. There was no difference in patient age, B-Raf expression, Ki67 immunostaining, or clinical stage at presentation between wild-type and BRAF V600E specimens. Immunodetection of phosphorylated and total forms of MEK and ERK revealed no difference in their phosphorylation between wild-type and BRAF V600E patient specimens or cell lines. Furthermore, a small inhibitory RNA construct targeting the expression of both wild-type B-Raf and B-Raf V600E induced a comparable reduction of viability in both wild-type and BRAF V600E mutant cancer cells. Interestingly, AAL881 inhibited MEK and ERK phosphorylation and induced apoptosis preferentially in BRAF V600E -harboring cells than wild-type ones, possibly because of better inhibitory activity against B-Raf V600E . We conclude that B-Raf is important for the pathophysiology of thyroid carcinomas irrespective of mutational status. Small molecule inhibitors that selectively target B-Raf V600E may provide clinical benefit for patients with thyroid cancer.

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Antitumor actions of cytokines on new human papillary thyroid carcinoma cell lines.

Cited by 29 publications

References 14 publications

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

Cytotoxic effects of a novel pyrazolopyrimidine derivative entrapped in liposomes in anaplastic thyroid cancer cells in vitro and in xenograft tumors in vivo

Targeting BRAFV600E in thyroid carcinoma: therapeutic implications

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